Regulation of Myocardial Blood Flow and Oxygen Delivery during Hypoxia

Abstract

The causes of cellular hypoxia can be classified by considering the flow of oxygen from air to tissues (Table 2-1). Arterial hypoxemia, anemia, and some of the abnormal hemoglobins jeopardize myocardial oxygen supply or delivery (defined as the product of arterial oxygen content and myocardial blood flow) by reducing the arterial oxygen content, and oxygen delivery must be maintained by an adequate increase in blood flow. If this cannot be achieved, oxygen extraction will have to be increased or else cell hypoxia will develop. Certain abnormal hemoglobins are associated with a normal arterial oxygen content but with a shift of P50 to the left that makes it harder to unload oxygen at the tissue level. Consequently, to avert cell hypoxia, blood flow has to increase so that myocardial oxygen delivery is above normal. Polycythemia or arterial stenosis tend to reduce myocardial blood flow for different reasons, but both may not only reduce myocardial oxygen delivery but also may lead to inadequate removal of metabolites. Finally, metabolic poisons such as cyanide, and perhaps those due to reperfusion injury, produce cell hypoxia in the face of a normal oxygen supply to organs; they will not be discussed further. For all of the other causes of cell hypoxia, the oxygen supply to the organs is deficient. The end result—cell hypoxia—is similar in all, but the associated features may depend on arterial oxygen tension, the oxygen dissociation curve, blood viscosity, and, for polycythemia and ischemia, on the inability of the reduced blood flows to remove metabolites adequately. In addition, associated responses of the sympathetic nervous system and its interactions with humoral agents may differ under different circumstances and lead to modifications of the basic myocardial responses (see Chapter 1, Circulatory Regulation during Hypoxia and Hypercapnia).